The mechanism regulating the onset of human parturition has been the subjet of intense investigation over the past decade, but remains one of the most elusive regulatory problems in reproductive physiology. Most studies have dealt with the control of uterine contractility but recently, emphasis has also been placed on the regulation of cervical softening and dilatation.
Existing animal models are not adequate to elucidate the human labor process. In animal species such as the sheep, the fetus plays a fundamental role in the physiological onset of labor. The signal for the spontaneous onset of labor is a rise in fetal plasma cortisol levels and this is followed by a fall in maternal progesterone and an increase in maternal estrogen concentrations. The change in the ratio of estrogens to progesterone seems to promote the release of prostaglandins from the placenta and other intrauterine tissues, and the prostaglandins stimulate uterine contractility and the onset of labor. In sheep, the integrity of the fetal pituitary and adrenal is essential for the spontaneous onset of labor, and the ovine placenta, under the influence of fetal cortisol, has the ability to convert progesterone to estrogen. This sequence of endocrine events is not detectable in human pregnancy.
Parturition in women occurs without apparent changes in either free or protein bound 17.beta.-estradiol and progesterone in plasms or in myometrial tissue. Maternal plasma levels of estradiol and progesterone have been measured in an attempt to predict which patients would deliver preterm, but this approach has failed.
Therefore, it seems likely that human parturition results from some signal or combination of signals, acting on inter-related endocrine and biochemical mechanisms, operating mainly with the uterus. These mechanisms probably operated within the decidua and fetal membranes, are established well before term, but are not normally activated until full term. Since the mechanism is still unknown, however, it has not heretofore been possible to reliably predict either the imminence of labor at term or the imminence of preterm labor.
Preterm labor occurs in little more than 5% of pregnancies but causes 85% of early neonatal deaths not associated with lethal fetal abnormality. One approach to the prediction of preterm labor has been to measure the contractions of the uterus in combination with the regular assessment of cervical dilatation and effacement. However, the validity of these procedures is in dispute. Vaginal examination in pregnancy has been shown to raise prostaglandin levels in the maternal circulation within minutes of this procedure. Since prostaglandins are known to be implicated in uterine contractility, repeated vaginal examinations might provoke preterm labor rather than helping to prevent it.
Furthermore, false positives in the prediction of preterm labor can cause undue anxiety for a large number of women and can lead obstetricians to intervene unnecessarily with "invasive" preventive measures such as tocolytic drugs or cervical cerclage. Since such interventions may themselves have dangers for either mother or fetus, the need for developing improved methods of discriminating women at risk of preterm birth is obvious.
Methods for the prediction of the imminence of term labor would also serve to relieve anxiety and would lead to improved medical care planning, particularly in the case of women who elect to travel in the third trimester.